With increasing parental age, there is an exponential increase in the frequency of children born with chromosomal disorders. Most studies indicate that this effect is chiefly due to maternal aging. We have developed a mouse model for examining this maternal age effect and have demonstrated a highly significant increase in the frequency of chromosomally abnormal fetuses with maternal aging. Studies conducted on mice have indicated that neither immunologic deficency nor genetic predisposition appear to play a strong role in the maternal age-related increase in chromosomally abnormal offspring. Current research is directed at examining other proposed etiologic agents for the maternal age effect as well as analyzing the potential role of paternal aging. The latter area is being approached by measuring the genetic complement of sperm samples obtained from members of the Baltimore Longitudinal Study.